Search results for: Hyperparathyroidism

Authors: Xiao-Li Dong, Quan-Gui Gao, Sa-Sa Gu, Hao-Tian Feng, Man-Sau Wong, Liya Denney

Abstract:

Postmenopausal osteoporosis is a disorder characterized by the progressive bone loss induced by estrogen deficiency in postmenopausal women. This imbalance affects calcium–phosphate metabolism and results in secondary hyperparathyroidism. Purariae Radix (PR), the root of P. lobata (Wild.) Ohwi, is one of the earliest medicinal herbs employed in ancient China. PR contains a high quantity of isoflavones and their glycosides, which are regarded as phytoestrogen. Few investigations of PR are related to its osteoprotective effects. The present study is designed to administer PR water extract to ovariectomized (OVX) female rats, for the investigation of its possibly protective actions on bone and to delineate the potential mechanisms involved. Our results demonstrated that long-term treatment of PR could not significantly improve bone properties, whereas it greatly ameliorated the condition of secondary hyperparathyroidism induced by ovariectomy in those animals. PR might be useful as alternative regimen for protecting against postmenopausal bone loss.

Keywords: Hyperparathyroidism, Ovariectomy, Postmenopausal Osteoporosis, Purariae Radix

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Authors: Surajit Debnath, Soma Addya

Abstract:

Human genome is not only the evolutionary summation of all advantageous events, but also houses lesions of deleterious foot prints. A single gene mutation sometimes may express multiple consequences in numerous tissues and a linear relationship of the genotype and the phenotype may often be obscure. ß Thalassemia minor, a transfusion independent mild anaemia, coupled with environment among other factors may articulate into phenotypic pleotropy with Hypocholesterolemia, Vitamin D deficiency, Tissue hypoxia, Hyper-parathyroidism and Psychological alterations. Occurrence of Pancreatic insufficiency, resultant steatorrhoea, Vitamin-D (25-OH) deficiency (13.86 ngm/ml) with Hypocholesterolemia (85mg/dl) in a 30 years old male ß Thal-minor patient (Hemoglobin 11mg/dl with Fetal Hemoglobin 2.10%, Hb A2 4.60% and Hb Adult 84.80% and altered Hemogram) with increased Para thyroid hormone (62 pg/ml) & moderate Serum Ca+2 (9.5mg/ml) indicate towards a cascade of phenotypic pleotropy where the ß Thalassemia mutation ,be it in the 5’ cap site of the mRNA , differential splicing etc in heterozygous state is effecting several metabolic pathways. Compensatory extramedulary hematopoiesis may not coped up well with the stressful life style of the young individual and increased erythropoietic stress with high demand for cholesterol for RBC membrane synthesis may have resulted in Hypocholesterolemia.Oxidative stress and tissue hypoxia may have caused the pancreatic insufficiency, leading to Vitamin D deficiency. This may in turn have caused the secondary hyperparathyroidism to sustain serum Calcium level. Irritability and stress intolerance of the patient was a cumulative effect of the vicious cycle of metabolic compromises. From these findings we propose that the metabolic deficiencies in the ß Thalassemia mutations may be considered as the phenotypic display of the pleotropy to explain the genetic epidemiology. According to the recommendations from the NIH Workshop on Gene-Environment Interplay in Common Complex Diseases: Forging an Integrative Model, study design of observations should be informed by gene-environment hypotheses and results of a study (genetic diseases) should be published to inform future hypotheses. Variety of approaches is needed to capture data on all possible aspects, each of which is likely to contribute to the etiology of disease. Speakers also agreed that there is a need for development of new statistical methods and measurement tools to appraise information that may be missed out by conventional method where large sample size is needed to segregate considerable effect. A meta analytic cohort study in future may bring about significant insight on to the title comment.

Keywords: Genetic disease, Genetic epidemiology, Heterozygous, Phenotype, Pleotropy, ß Thalassemia minor, Metabolic compromises.

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